Blaming the Brain for Chronic Back Pain

The vast majority of adults have had a sore back at some point in their lives. If they're lucky, the pain subsides after a few days or weeks. But for some, whose initial injuries appear no different than the fortunate ones, back pain lasts for years. Now, researchers have discovered a difference in brain scans between the two groups of patients that appears early in the course of the pain. The finding could lead to not only ways of identifying patients who are the most at risk for long-term pain but to new treatments or preventions for chronic pain.

"This is the very first time we can say that if we have two subjects who have the same type of injury for the same amount of time, we can predict who will become a chronic pain patient versus who will not," says neuroscientist Vania Apkarian of Northwestern University, Chicago, who led the new work.

Over the past 2 decades, Apkarian's lab has run many studies comparing the brains of patients with chronic back pain with those of healthy people, finding differences in brain anatomy or the function of certain regions. But the study designs made it hard to sort out which brain changes were consequences of the chronic pain—or the patients' painkillers or altered lifestyles—versus those that drove the pain's chronic nature.

Apkarian and colleagues have now tracked the brains of back pain patients over time rather than comparing single neural snapshots. His team began with 39 people who had experienced moderate back pain—a five or six on a self-described scale of 10—for 1 to 4 months. Over the next year, the team scanned the patients' brains four times and followed their pain. By year's end, 20 of the patients had recovered, while 19 continued to hurt, meeting the criteria for chronic pain.

The scientists then looked at a number of brain characteristics, including the amount of communication between two areas of the brain previously seen to have altered activity in back pain patients: the insula and the nucleus accumbens. These regions are involved in emotional responses to a person's environment and in how the brain learns. Not only did they measure more communication between the two areas in chronic back pain patients than in those whose pain subsided, but the increased crosstalk could be seen as far back as the start of the study, suggesting that it could have predicted which patients would suffer the whole year. But further work will need to confirm that the scans have predictive value.

"Our interpretation of the results is that how these areas of the brain engage with the injury then dictates how the rest of the brain is going to reorganize," says Apkarian. It underscores that brain regions involved in learning and emotions are important in the development of chronic pain, he says, not just brain regions directly responsible for sensing pain.

"This is a transformative piece of work," says neurologist David Borsook of Harvard University, who was not involved in the study. "Finding that these changes are predictive is very exciting."

Borsook says more research is needed to completely sort out what makes pain chronic; the new finding is likely only one piece of the puzzle. "We're still not sure when acute pain transforms to chronic pain," he says. "We use these arbitrary time points." And the results need to be repeated with different patient populations and study designs to gain traction within the field, he says. But the new study is a step on the way to having quantitative ways of defining pain by using scans, rather than relying on descriptions of the pain from patients.

"This is a fantastic thing for the field of pain imaging," Borsook says, "and I have no doubt that this same data set holds other findings about chronic pain that we will learn about in the near future."